Expression of caps^Scer\UAS.cSa in both R7 and R8 photoreceptors, under the control of Scer\GAL4^sev.PM181, generates an R7 axon stopping phenotype.

Expression of caps^Scer\UAS.cSa in R7 and R8 photoreceptors, under the control of Scer\GAL4^GMR.PF, in a transheterozygous caps^C28fs/Df(3L)Exel6118 background display the same R7 mistargeting phenotype as found upon expression of caps^Scer\UAS.cSa in a wild-type background.

Expression of caps^Scer\UAS.cSa under the control of Scer\GAL4^unspecified in anterodorsal or lateral projection neuron neuroblast clones results in severe dendrite mistargeting defects, resulting in deformation of the entire antennal lobe structure.

Expression of caps^Scer\UAS.cSa under the control of Scer\GAL4^Mz19 results in a mistargeting of projection neuron dendrites to the VA1lm glomerulus (81%) and the VA4 glomerulus (31%). This results in a segregation of the dendritic field of the Scer\GAL4^Mz19-positive projection neurons to nonadjacent regions in the antennal lobe, in contrast to the continual dendritic field of Scer\GAL4^Mz19-positive projection neurons that is seen in control flies.

Single-cell DL1 projection neuron clones expressing caps^Scer\UAS.cSa under the control of Scer\GAL4^GH146 show partial loss of innervation of the DL1 glomerulus and mistargeting of dendrites to ectopic glomeruli, which are mostly normally innervated by caps-positive projection neurons. Over two-thirds of the mistargeting events occur at glomeruli near DL1 (DL2d, DL2v, VL2a and VL2p), suggesting that mistargeting is preferentially local. The mistargeting may not be random among local targets, as two local glomeruli (DL4 and DL5) have no mistargeted dendrites.

Expression of caps^Scer\UAS.cSa in DL1 projection neurons under the control of Scer\GAL4^GH146 causes dendrites to extend across the midline of the dorsomedial-ventrolateral axis of the antennal lobe in approximately 40% of cases at 16 hours after puparium formation (APF). This medial mistargeting phenotype persists at 48 hours APF.

The dendrite targeting defects of single-cell DL1 projection neuron clones expressing caps^Scer\UAS.cSa under the control of Scer\GAL4^GH146 are still seen in a caps^C28fs/Df(3L)Exel6118 background.

Expression via Scer\GAL4^fkh.PH results in salivary glands with an enlarged lumen and very aberrant shapes at embryonic stage 15. During early stages of invagination, the invagination hole appears enlarged compared to wild type and extended along the anterior-posterior axis.

caps^Scer\UAS.cSa; Scer\GAL4^how-24B embryos show a high frequency of ISNb phenotypes, in particular 70% have a distinctive 'loop-back' phenotype in which which an axon from ISNb forms a terminal loop with its distal tip at muscle 13.

Embryos that express caps^Scer\UAS.cSa under the control of Scer\GAL4^twi.PG show dorsal trunk interruptions at several fusion points. Some of the truncated dorsal trunk branches travel in abnormal directions instead of fusing with their adjacent targets. There are more breaks in the dorsal trunk at stage 14 than at later embryonic stages. When caps^Scer\UAS.cSa is overexpressed in mesodermal cells surrounding the lateral trunk, a discontinuous lateral trunk is formed.

Expression of caps^Scer\UAS.cSa under the control of Scer\GAL4^GMR.PY results in 82% of the R7 photoreceptor axon terminating in the M3 layer of the medulla (where the R8 axons terminate in wild type). It appears that the R7 axons initially target to the correct layer in the medulla in early pupae, but then retract back to the M3 layer during mid-pupal development. Targeting of the R1-R6 axons to the lamina appear largely normal in these animals.

Medially located somatic clones of caps^Scer\UAS.cSa; Scer\GAL4^Act5C.PP cells in the wing disc adopt more rounded shapes at the control clones. When such clones were laterally located they were more elongated than medial clones, but still had much smoother borders than equivalently located wild-type control clones.

Fewer clones expressing caps^Scer\UAS.cSa under the control of Scer\GAL4^Act5C.PP are recovered in the ventral compartment of the wing disc compared to the dorsal compartment. Twice as many clones are recovered at the dorsal/ventral boundary as would be expected if expression of caps had no affect on their distribution. Wing disc clones expressing caps^Scer\UAS.cSa under the control of Scer\GAL4^Act5C.PP that bisect the nascent dorsal/ventral boundary (these clones are induced in the wing disc in the early 2nd instar before the dorsal/ventral boundary forms) are more compact in shape and have smoother borders compared to control clones and are often considerably smaller in the ventral compartment than the dorsal compartment. Cells in ventral clones in the wing disc expressing caps^Scer\UAS.cSa under the control of Scer\GAL4^Act5C.PP extend processes towards the dorsal compartment.

Third instar larvae expressing caps^Scer\UAS.cSa under the control of Scer\GAL4^elav.PLu at 29^oC have no gross morphological defects in the central nervous system or musculature. The trajectory of the motorneurons that innervate muscle 12 is altered; they pass along the exterior of muscle 13 in 29% of hemisegments, in contrast to wild-type larvae where they project along the internal surface of muscle 13 before reaching muscle 12. The mutant motorneurons do reach their normal target by turning interiorly at the cleft between muscles 12 and 13 and establish normal synapses on muscle 12. The penetrance of the phenotype depends on the level of ectopic caps expression. Defects in ISNb morphology are first seen in embryos expressing caps^Scer\UAS.cSa under the control of Scer\GAL4^elav.PLu at 29^oC during late stage 16 to early stage 17 at its distal edge. In 18% of hemisegments, a misrouting phenotype similar to that seen in larvae is observed. In 13% of hemisegments the terminal branch of ISNb stalls near muscle 30. Occasionally, thin axonal processes are seen to emanate from the stalled nerve terminal, which stop prematurely and fail to innervate muscle 12. Larvae expressing caps^Scer\UAS.cSa under the control of Scer\GAL4^elav.PLu also show defects in transverse nerve formation. The nerve is often split and the cell body of the lateral bipolar cell (which is associated with the transverse nerve) is occasionally mislocated. The subbranches of the intersegmental nerve b (ISNb) that terminate on ventral muscles other than muscle 12 show no abnormalities in their trajectory or targeting. The ISN, ISNd, segmental nerve a (SNa) and SNc have normal morphology. Expression of caps^Scer\UAS.cSa under the control of Scer\GAL4^how-24B results in the terminals of motorneurons that normally innervate muscle 12 forming ectopic synapses on muscle 13 in 40% of hemisegments.

When expression is driven by Scer\GAL4^G14, muscle development and adhesion are unaffected, but ectopic synapses form. In approximately 70% of the hemisegments the ISNb terminal formed one or more additional collateral that formed on more robust synaptic endings on muscle 13. When expression is driven by Scer\GAL4^Mhc.PW, no ectopic endings from ISNb form. When expression is driven by Scer\GAL4^l(3)H94-H94, ectopic endings develop from ISNb on muscle 13, in addition to normal synapses forming on muscle 12.